Inappropriate Elevation of the Aldosterone/Plasma Renin Activity Ratio in Hypertensive Patients with Increases of 11-Deoxycorticosterone and 18-Hydroxy-ll-Deoxycorticosterone: A Subtype of Essential Hypertension?

Cardiology ◽  
1991 ◽  
Vol 78 (2) ◽  
pp. 99-110 ◽  
Author(s):  
Ichiro Komiya ◽  
Takashi Yamada ◽  
Toru Aizawa ◽  
Nobuyuki Takasu ◽  
Akihiro Niwa ◽  
...  
1976 ◽  
Vol 51 (s3) ◽  
pp. 185s-188s ◽  
Author(s):  
G. W. Thomas ◽  
J. G. G. Ledingham ◽  
L. J. Beilin ◽  
A. N. Stott

1. Supine plasma renin activity and its responsiveness to erect posture and frusemide were reduced in fifty-one patients with essential hypertension, compared with fifty-one age- and sex-matched control subjects. 2. Twenty-four hour urinary sodium excretion was similar in hypertensive patients and control subjects, but after intravenous frusemide hypertensive patients excreted significantly less sodium. 3. A significant inverse relationship between plasma renin activity and diastolic blood pressure was demonstrated in hypertensive patients and in normotensive control subjects. 4. A significant inverse relationship between plasma renin activity and age, independent of blood pressure, was shown in hypertensive patients and control subjects. 5. It is concluded that the reduced renin values found in essential hypertension are, in part, the result of the elevated blood pressure acting on the kidney.


1975 ◽  
Vol 49 (5) ◽  
pp. 511-514
Author(s):  
J. Chodakowska ◽  
K. Nazar ◽  
B. Wocial ◽  
M. Jarecki ◽  
B. Skórka

1. The effect of physical exercise on blood pressure, plasma catecholamines and plasma renin activity was studied in fourteen patients with essential hypertension and in eight healthy subjects. 2. Resting plasma noradrenaline and adrenaline and plasma renin activity of the hypertensive patients did not differ from those of the control subjects. 3. In response to graded exercise producing successive heart rates of 120, 140 and 160 beats/min, significantly greater increases of blood pressure were found in the patients than in the control subjects. 4. Plasma noradrenaline increased significantly in both groups at all levels of exercise, the responses being significantly greater in the hypertensive patients. 5. The mean arterial blood pressure was significantly correlated with plasma noradrenaline concentration in the control subjects but not in the hypertensive patients. 6. In the hypertensive group plasma adrenaline increased significantly after exercise at all work loads whereas, in the control group, significant increase occurred only at the highest work load. The differences in the response of the two groups were significant at each work load. 7. Plasma renin activity increased significantly after exercise at the heart rate of 120 beats/min, both in the hypertensive patients and in the control subjects. The magnitude of the response was similar in the two groups.


1974 ◽  
Vol 48 (s2) ◽  
pp. 77s-79s
Author(s):  
G. Leonetti ◽  
G. Mayer ◽  
A. Morganti ◽  
L. Terzoli ◽  
A. Zanchetti ◽  
...  

1. Stepwise increases of oral doses of propranolol produced both a significant lowering of blood pressure and suppression of plasma renin activity in sixteen patients with mild or moderate normal-renin essential hypertension. 2. The hypotensive and the renin-suppressive actions of propranolol were differently related to plasma propranolol concentrations. At the lowest propranolol concentrations (15–40 nmol/l), there was almost no decrease in blood pressure whereas plasma renin activity and responsiveness to renin-releasing stimuli (standing, intravenous frusemide) were already strongly depressed (greater than 50%). Therefore in a large number of normal-renin hypertensive patients under small doses of propranolol, the renin-suppressive action of the drug can be dissociated from the hypotensive effect. Dissociation of the two effects, though in the opposite way, was also observed in three of four low-renin hypertensive patients, whose blood pressure was decreased by propranolol without further reduction of the already suppressed plasma renin activity. 3. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, the hypotensive effect of propranolol cannot be attributed to suppression of renin activity. These conclusions do not necessarily apply to high-renin hypertensive patients.


1974 ◽  
Vol 48 (s2) ◽  
pp. 85s-88s ◽  
Author(s):  
G. Muiesan ◽  
C. Alicandri ◽  
E. Agabiti Rosei ◽  
M. Motolese ◽  
C. Valori

1. Catecholamine plasma concentrations and urinary excretion were measured together with plasma renin activity in ten patients with essential hypertension and in five normal control subjects before and after a frusemide challenge. 2. The same procedure was repeated in the same subjects 3–4 days later after pretreatment with oxprenolol. 3. Noradrenaline plasma concentrations and urinary excretion increased significantly after frusemide in all cases, returning to normal values at 30 and 60 min. Adrenaline plasma concentrations and urinary excretion were unchanged. 4. Plasma renin activity increased significantly in seven patients with hypertension and normal renin basal values, remaining unchanged in three hypertensive patients with low-renin basal values. 5. Oxprenolol suppressed the response of noradrenaline and plasma renin activity to frusemide in all cases.


1978 ◽  
Vol 55 (1) ◽  
pp. 51-55 ◽  
Author(s):  
A. Lechi ◽  
G. Covi ◽  
C. Lechi ◽  
A. Corgnati ◽  
E. Arosio ◽  
...  

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroups: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients β-adrenoreceptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.


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